Bunyaviruses are a family of segmented, negative-sense RNA viruses transmitted globally by arthropod vectors. Several members are emerging pathogens that pose significant threats to human and animal health, with severe infections leading to haemorrhagic fever, encephalitis, and death. Despite their clinical importance, bunyaviruses remain relatively understudied, and effective treatment strategies are lacking. Stress granules (SGs) are cytoplasmic biomolecular condensates that form in response to cellular stress, such as viral infection, and are thought to provide a platform for enhanced innate immune signalling. Many viruses have evolved mechanisms to disrupt SG formation to promote viral replication and spread; however, the interaction between bunyaviruses and the host cellular stress response is poorly characterized. Here, we characterise the interaction between the prototype bunyavirus Bunyamwera virus (BUNV) and host cell stress response pathways in both neuronal and non-neuronal cell models. We show that BUNV induces activation of the integrated stress response (ISR) and promotes SG formation in multiple cell types. Furthermore, we demonstrate that the non-structural protein S (NSs) alters SG morphology and function. In addition, we have established a human cerebral organoid model to study bunyavirus infection in a physiologically relevant system. Using this model, we can characterise the neurotropism of BUNV and further dissect host–virus interactions within the central nervous system. Overall, our findings reveal that Bunyamwera virus modulates host stress response pathways across diverse cellular models and suggest a novel role for NSs in regulating SG biology. These results provide new insights into how bunyaviruses interact with antiviral stress signalling.